Document Type

Article

Publication Date

7-1-2018

Comments

This article has been peer reviewed. It is the author’s final published version in Neurology: Neuroimmunology and NeuroInflammation, Volume 5, Issue 4, July 2018, Article number e460.

The published version is available at https://doi.org/10.1212/NXI.0000000000000460. Copyright © Rakocevic et al.

Abstract

Anti-MAG demyelinating neuropathy is difficult to treat. All immunotherapies have failed except for rituximab, a chimeric B-cell–depleting monoclonal antibody against CD20, that helps up to 40% of patients based on 2 controlled and several uncontrolled series.1,–,3 Because the majority of these patients are left disabled, stronger anti–B-cell agents might be promising.

We describe clinical response and autoantibody changes after treatment with obinutuzumab (Gazyva), a new generation of humanized anti-CD20 monoclonal antibodies, in 2 patients with anti-MAG neuropathy who continued to worsen despite multiple courses of rituximab. Obinutuzumab, approved for chronic lymphocytic leukemia (CLL), exerts greater peripheral and lymphoid B-cell depletion4 and might be more effective in rituximab-refractory patients. © Rakocevic et al.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

PubMed ID

29629397

Language

English

Included in

Neurology Commons

Share

COinS